Cardiology ACS + SHOCK Flashcards

(39 cards)

1
Q

On rapid review of chest pain, what life threating conditions are you trying to assess for?

A
  • acute coronary syndrome
  • aortic dissection
  • pulmonary embolism
  • severe pneumonia
  • tension pneumothorax
  • eosphageal rupture
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2
Q

How long should it take for anginal pains to go away?

A

2 -10 min

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3
Q

In what patient population is atypical chest pain with ACS seen in?

A
  • women
  • racial minorities
  • diabetics
  • elderly
  • pts with psychiatric illness
  • alerted mental state
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4
Q

What features on a CXR are you looking for in a pt suspsected of an eosphageal rupture?

A
  • Pleural effusion (left more common than right)
  • pneumomediastinum
  • pneumoperitoneum
  • subcutaenous emphysema

normal CXR cannot exclude diagnosis though

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5
Q

what are risk factors for an aortic dissection?

A
  • age > 50
  • male
  • atherosclerosis
  • poorly controlled HTN
  • cocaine or amphetamine use
  • biscuspid aortic valve
  • aortic valve replacement
  • connective tissues disorder (marfan’s, Ehler-Danlos)
  • pregnancy
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6
Q

What investigation findings might be abnormal in pt with an aortic dissection (exclude the CT aortogram)

A
  • ECG:ST elevation/depression or TW changes ( 50%)
  • positive D-dimer (not diagnostic and normal does not exclude)
  • Elevated troponin (increased mortality)
  • blood suggestive of end organ ischaemia: AKI, transaminitis, elevated lactate
  • widened mediastinum, double aortic or irregular contour
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7
Q

What examination findings might be present in someone with a ruptures eosphagus?

A
  • subcutaneous emphysema of the neck
  • Hamman’s crunch
  • tachycardia
    -tachypnoea
  • febrile
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8
Q
A
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9
Q

What CT do you order to look for a eosphageal rupture?

A

CT chest with oral contrast 20 minutes before (to demonstrate extraluminal contrast leak) and IV contrast to delineate eosophageal wall

mortality rate 25 - 50%

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10
Q

What % of patients < 40 years old without known coronary artery disease with a normal ECG have ACS?

A

< 1%

in other age groups however ECG cannot exclude ACS, up to 10% with ACS may have a normal ECG or ECG may be misinterpretted as normal

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11
Q

How long after myocardial infarction does it take for troponin to peak and how long till it is undetectable?

A

Peak 1 day
Levels back to normal 7 days

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12
Q

What is the sensitivity to detect ACS with two high sensitivity troponins take within 2-3 hrs of ED arrival?

A

Nearly 100%

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13
Q

bradyarrhythmias are more common in ACS in what region of the heart?

A

inferior

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14
Q

Which extra heart sound is heard in 15 - 20% of AMIs

A

S3

Heard in early diastole immediately after S2. Due to rapid ventricular filing such as from a dilated ventricle or volume overload from valvular regurgitation

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15
Q

A new systolic murmur in the setting of AMI may be from what?

A
  • papillary muscle dysfunction
  • flail mitral valve leaflet causing MR
  • ventricular septal defect

ominous sign

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16
Q

A pt has a NSTEMI and have ongoing pain after one hour. You have tried GTN, and fentanyl and given DAPT and enoxparin. What is you next treatment option?

A

DW cardiology to consider reperfusion. PCI or thrombolysis

At minimum need to start tranfering to hospital that can do PCI
Can also consider GTN infusion, low dose e.g 10mcg/min and tirate to 10% reduction in MAP if normotensive and 30% reduction if HTN

17
Q

In what time frame is reperfusion therapy for a STEMI indicated?

A

12 hours
Can consider > than 12 hours if signs of ongoing ischaemia, viable myocardium or major complications

18
Q

A pt has a STEMI and is going for PCI. What is the preferred second antiplatelet, route and dose?

A

Ticagrelor 180mg PO loading dose
Prasugrel 60mg PO loading dose

19
Q

What are the contraindications to ticagrelor?

A
  • active pathological bleeding
  • prior intracranial haemorrhage or stroke, recent gastrointestinal bleeding or anaemia, or has a coagulopathy
  • severe hepatic impairment
  • has a high or very high bleeding risk HAS-BLED score of more than 3
  • co-administration with strong CYP3A4 inhibitors e.g. ketoconazole, clarithromycin, nefazodone, ritonavir, atazanavir.
20
Q

what 9 variables make up the HAS-BLED score

A
  • HTN
  • renal disease
  • Liver disease
  • stroke history
  • prior major bleadig or predisposition to bleeding
  • labile INR
  • Age > 65
  • Medication use predisposing to bleeding
  • Alcohol use

Uncontrolled HTN = SBP > 160
Renal disease = creat > 200, HD, transpant
Liver disease = cirrhosis or bilirubin > 2x normal as tranasaminitis > 3x normal
Unstable INR= Unstable/high INRs, time in therapeutic range < 60%
Alcohol use = ≥8 drinks/week

21
Q

What are the absolute contrainications to thrombolysis

HINT: there are 7

A
  • Any prior intracranial haemorrahge
  • Known structural cerebrovascular lesion
  • Known malignant intracranial neoplasm
  • Ischaemic stroke within 3 months
  • Susected aortic dissection
  • Active bleeding or bleeding diathesis
  • Significant closed head or facial trauma within 3 months

Menses do not count as bleeding
DW cardiology. Consider PCI or half dose thrombolysis

22
Q

Name 5 relative contraindications to thrombolysis

A
  • chronic severe poorly controlled HTN
  • BP >180/110mmHg
  • Ishcaemic stroke more than 3 months ago, dementia or intracranial abnormality not considered an absolute contraindication
  • TIA within last 6 months
  • traumatic or prolonged CPR (>10 min)
  • Recent major surgery (within 3 weeks)
  • Recent internal bleeding (within 4 weeks)
  • Noncompressible vascular puncutres within last 24 hours (e.g LP, liver biopsy)
  • pregnancy or within 1 week postpatum
  • active peptic ulcer disease
  • current use of anticoagulants
  • advanced liver disease
  • infective endocarditis

DW cardiology. Consider PCI or half dose thrombolysis

23
Q

What is the dose of tenectaplase for each weight group:

less than 60 kg:

60 to 69 kg:

70 to 79 kg:

80 to 89 kg:

90 kg or more:

A

less than 60 kg: 30 mg (6000 units) intravenously

60 to 69 kg: 35 mg (7000 units) intravenously

70 to 79 kg: 40 mg (8000 units) intravenously

80 to 89 kg: 45 mg (9000 units) intravenously

90 kg or more: 50 mg (10 000 units) intravenously.

24
Q

What is those of enoxparin as part of thrombolysis treatment for the following groups:

younger than 75 years and CrCl 30 mL/min or more:

younger than 75 years and CrCl less than 30 mL/min:

75 years or older and CrCl 30 mL/min or more:

75 years or older and CrCl less than 30 mL/min:

A

Younger than 75:
- both get 30 mg IV enoxaparin
- good kidneys 15 min later get 1mg/kg SUBCUT 12 hrly (max 100mg)
- bad kidneys 15 in later 1mg/kg SUBCUT 24 hlry (max 100mg)

Older than 75:
- NO IV ENOXAPARIN
- good kidneys 0.75mg/kg enoxparin SUBCUT 12 hlry (max 75mg)
- bad kidneys 1mg/kg enoxaparin SUBCUT 24 hrly (max 75mg)

25
Your pt has very poor renal function and a hx of GI bleed 6 months ago. You have chosen to treat their ACS with heparin. What is the loading dose and starting infusion rate?
60units/kg max 4000 units IV then 12units/kg/hr up to 1000 units/hr ## Footnote Adjust according to APTT
26
You have having given a pt therapeutic enoxparin. They developed a headache and on CT you see that have bleed. What agent can you use to help reverse enoxaparin. Name drug, route and dose
- protamine, IV - if < 8 hrs of last dose 1mg per 1mg of enoxparin (max 50mg - if > 8 hrs 0.5mg per 1mg enoxparin (max 50mg) ## Footnote e.g if 80mg subcut clexane given 2 hours ago, dose = 50g IV protamine. If given 10 hours ago dose = 40mg Will reverse 60 - 75% of anticoagulant effect of LMWH Protamine can cause hypotension, flushing, pulmonary oedema and bradycardia. It is a derivative of fish sperm, and can cause anaphylaxis; however, the benefit of protamine in a patient with clinically significant bleeding outweighs the risk of an allergic reaction. The risk of an allergic reaction increases in patients who have developed preformed antibodies, including those patients who: have previously received protamine (eg during coronary artery bypass grafting [CABG] surgery) use, or have used, protamine insulin are allergic to fish have had a vasectomy.
27
Why is it critical that patients get an antithrombin (i.e enoxaparin) and antiplatelets when getting thrombolysis?
As the thrombus is broken down thrombin is exposed which is a potent platelet activactor ## Footnote despite this thrombolysis for STEMI's failed in 40 - 50% of pts 0.5 to 1% risk of cerebral haemorrhage
28
What reduction in mortality does giving aspirin to a STEMI pt achieve?
23% ## Footnote don't withold for minor contraindications
29
The combination of heparin and aspirin was shown to reduce death in pts with unstable anging by what %
56% ## Footnote This is why antiplatelets and heparin are given to STEMIs. in NSTEMIs enoxaparin is favoured due to ease of dosing and reliable effect
30
In addition to relaxing smooth muscle in ateries, vein, including coronary vessels. What secrete power does GTN have that also helps treat AMI's?
It has an antiplatelet effect
31
Nitrates have been shown to reduce mortality by 35% but what is the end goal that was used in these studies?
BP reduction - reduce MAP by 10% if normotensive - reduce MAP by 35% if HTN ## Footnote End goal was not symptom resolution Use BP target is using an infusion
32
What is a contraindication to using GTN?
- phosphodiasterase inhibitors: sildenafil within 24 hours or tadalafil within 48 hours - right sided infarction **caution in inferior infarction as may be extending to right** - and obviously hypotension or allergy
33
Why is correcting hypomagnesaemia important with AMI?
- causes systemic vasodiation (reduced afteroad) - causes coronary dilation - suppressed automaticity - antiplatelet effect - protects myocytes from calcium influx during reperfusion
34
How would you treat a patient you has been diagnosed with a NSTEMI then goes into AF with mild compromise?
- could shock - or if only mild decompensatoin, could give amiodarone ## Footnote if completely stable can treat as per usual (beta blockers, digoxin, magnesium ect)
35
You gave a pt atropine because they had a sinus bradycardia in the setting of an AMI. The cardiologist was upset as they said they had a normal BP and did not needed it. Why should you be cautious with atropine use in AMI?
- the parasympathetic tone (the is now blocked) is proctective against infarct extension and VF. Atropine will increaes HR and afterload ## Footnote Use only if haemodynamics are compromised
36
You are doing your ICU rotation and attend a MET call for a pt who has been admitted for 2 days with an NSTEMI. They have been stable but suddenly decompensated. What three diagnoses that are specific to AMI should you think of?
- ventricular free wall rupture (will be in tamponade) - rupture of interventricular septum (new holosystolic murmur) - papillary muslce rupture (inferior AMI, sudden mitral regurg with APO) ## Footnote Treatment of all is surgical also of course consider PE or arrhythmia
37
You diagnosed a pt with pericarditis. The pt tells you they have a NSTEMI 2 weeks ago. Why is ibuprofen contraindicated?
Interferes with antiplatelet action of asprin and can cause myocardial scar thinning ## Footnote Treat dressler's syndrome with aspirin or colchicine
38
What are the principles of treating a right sided infarction (do's and don't for drugs, goals for the do's and don't)
- **Increase preload**: consider 1 L saline load - **Don't decrease preload**: diuretic, GTN - improve inotropy without increaseing afterload: dobutamine studied most (2.5 - 40mcg/kg/min) - **decrease afterload** without decreasing preload. Give sodium nitroprusside. It dilate veins and arteries but less venodilation than GTN (don't want venodilation) ## Footnote dobutamine causes less vasoconstriction then adrenaline and less inotropy than adrenaline
39
What time frame is each stent most at risk for re-stenosis: - bare metal stent - drug eluting stent
- bare metal: 2 -14 days - drug eluting: delayed 9 -12 months, often when clopidogrel ceased ## Footnote Symptoms are ACS after stent placemet, assume stent has stenosis. CABG grafts can also stenose post operatively